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At least 109 records · Page 6Linked to original sources
PubMed1990

Accelerated recovery from gamma-irradiation-induced leukopenia in mice by the biscoclaurine alkaloid, Cepharanthin--comparison with recombinant human granulocyte colony-stimulating factor.

The effect of a biscoclaurine alkaloid drug, Cepharanthin (CE), on recovery from severe leukopenia induced by whole body gamma-irradiation at a dose of 3 Gy, was compared with that of recombinant human granulocyte colony-stimulating factor (rhG-CSF). Daily intraperitoneal administration of 100 micrograms CE into the irradiated mice significantly prevented decrease of leukocyte numbers in the peripheral blood and accelerated recovery from leukopenia to normal. The activity of CE was somewhat weaker than that of 20,000 units of rhG-CSF when administered daily subcutaneously. In cell composition of peripheral leukocytes, CE increased the numbers of polymorphonuclear (PMN) cells and lymphocytes compared with those of the irradiated controls. Stronger change in PMN cell numbers than with CE was induced by administration of rhG-CSF. No significant increment of the activity to form colonies in spleen (colony-forming unit in spleen; CFU-S) was observed in bone marrow cells from irradiated donor mice administered CE, though CE induced CSF production into sera. Administration of rhG-CSF stimulated the CFU-S activity. These results indicate that CE increased recruitment of PMN cells from the marginal pool rather than the stimulation of pluripotent stem cells in the bone marrow.

Alkaloids↗
PubMed1990

Efficacy and tolerability of recombinant human granulocyte-macrophage colony-stimulating factor in patients with chemotherapy-related leukopenia and fever.

30 patients with chemotherapy-related leukopenia (white cells 1.0 x 10(9)/l or lower) and fever (temperature 38.5 degrees C or higher) were treated in a double-blind randomised trial with standard antibiotics and 7 days of intravenously administered recombinant human granulocyte-macrophage colony-stimulating factor (GM-CSF, 2.8 micrograms/kg per day) or placebo. GM-CSF administration resulted in a faster percentage increase of peripheral neutrophil count after 2 and 3 days of treatment, except in patients treated with ablative chemotherapy and autologous bone-marrow transplantation. However, GM-CSF did not shorten the period of fever or antibiotic administration. No side-effects were observed; in particular tumour necrosis factor alpha and interleukin-6 did not increase in the 5 GM-CSF patients tested. These data suggest that a subgroup of patients with chemotherapy-related leukopenia and fever may benefit from GM-CSF treatment in view of the observed effects on neutrophil count.

Adolescent↗
PubMed2005

Severe leukopenia and liver biochemistry changes in adult rabbits after calicivirus infection.

Calicivirus infection is the major cause of the severe decrease in the stocks of wild and farm rabbits that has occurred worldwide during the last two decades. Adult rabbits (10-weeks-old) were experimentally infected with a calicivirus inoculum that killed all animals by causing rabbit haemorrhagic disease (RHD) within 24-62 h of infection. The rabbits were used to evaluate blood cell numbers and serum biochemistry every 6h, starting 12h after the inoculation of the caliciviruses. No significant changes in blood parameters were observed in most of the rabbits up to 18 h of infection. Severe leukopenia was seen 6h before death of the infected rabbits; both heterophils and lymphocytes contributed to the decrease in circulating white blood cells. Platelets were also severely decreased in number. Marked enhancement in liver enzymes was seen 6-12 h before death of the infected rabbits. There was also evidence both for cholestasis, as expressed by the elevated levels of direct (conjugated) bilirubin, and for hypoglycemia, an alteration that it is likely to contribute for the seizures that rabbits show during the late stages of RHD. Liver ultrastructure of rabbits that died from RHD revealed extensive hepatocyte vacuolization, severe changes in mitochondrial structure, and depletion of glycogen granules. We conclude that: (i) severe leukopenia characterizes the final hours of calicivirus-induced RHD; (ii) hypoglycemia and cholestasis precede death of rabbits from RHD; (iii) the kinetics of liver enzymes allows an accurate prediction of the time of death of rabbits from calicivirus-induced RHD.

Animals↗
PubMed1980

The effect of lithium carbonate on leukopenia after chemotherapy.

To evaluate the efficacy of lithium carbonate in ameliorating leukopenia, 37 patients (3 to 26 years old, mea (less than or equal to 1,000/mm3) over 40% of the time were designated at random on the last day of 82 separate chemotherapy courses to receive lithium or no treatment. Four could not take the drug because of the size of the capsules. There were 39 controls and 39 patients given lithium. Blood levels were maintained at 0.2 to 1.2 mEq/1 (median 0.7). The median drop of WBC in the treated group was 3,400/mm3 with a nadir of 1,800/mm3 vs 5,000 and 1,400, respectively, for the untreated patients (P LESS THAN 0.01). Eight patients (21%) in the lithium-treated group became severly leukopenic (less than or equal to 1,000/mm3) while 14 (36%) in the control group became leukopenic to that extent. Twenty-four patient days were spent with the WBC less than or equal to 1,000/mm3 after lithium and 57 days in the control group. Three patients required admission for 24 hospital days for fever while leukopenic after lithium, whereas seven patients spent 62 days in the hospital in the control group. Lithium reduces the period of leukopenia after chemotherapy during which time the patients may acquire infections.

Adolescent↗
PubMedDate not supplied

Clinical study of the effect of the preparation DEODAN on leukopenia, induced by cytostatics.

The aim of the study is to establish the effect of the preparation DEODAN on leukopenia induced by chemotherapeutics in oncological patients. DEODAN is an oral preparation, obtained from lyzozyme lysates of Lactobacillus bulgaricus strain "I. Bogdanov patent strain tumoronecroticance B-51" ATCC 21815, called shortly LB51. In the study there are included two groups of patients--from National Oncological Centre, Sofia, the other from Clinic of Medicine, Bertha Academic Hospital, Clinics of Duisburg, Duisburg. All the patients, (78) have undergone combined chemotherapy. In all patients, leukopenia has been established in moderate and medium levels. The scheme of the application of DEODAN has been 3 g, three times a day before meals, from the first day of establishing the disturbances of the haemopoesis. The treatment lasted until the restoration of the haematological values. Only DEODAN was applied. The results obtained show that the recovery of the WBC count (values above 3000) took place in all of the patients between days 3 and 5. None of the patients displayed any infectious or febrile complications, as a result of the applied chemotherapy and the treatment with the preparation. DEODAN also improves the general condition of the patients.

Administration, Oral↗
PubMed2000

Treatment of chemotherapy-induced leukopenia in a rat model with aqueous extract from Uncaria tomentosa.

The Uncaria tomentosa water extracts (C-Med-100) depleted of indole alkaloids (< 0.05%, w/w) have been shown to induce apoptosis and inhibit proliferation in tumor cells in vitro and to enhance DNA repair, mitogenic response and white blood cells in vivo. In this study, the effect of C-Med-100 in the treatment of chemically induced leukopenia was evaluated in a rat model. W/Fu rats were treated first with doxorubicin (DXR) 2 mg/kg x 3 (i.p. injection at 24 hour-intervals) to induce leukopenia. Twenty-four hours after the last DXR treatment, the rats were daily gavaged with C-Med-100 for 16 consecutive days. As a positive control, Neupogen, a granulocyte colony stimulator was also administered by subcutaneous injection at a dose of 5 and 10 microg/ml for 10 consecutive days. The results showed that both C-Med-100 and Neupogen treatment groups recovered significantly sooner (p < 0.05 by Duncan test) than DXR group. However, the recovery by C-Med-100 treatment was a more natural process than Neupogen because all fractions of white blood cells were proportionally increased while Neupogen mainly elevated the neutrophil cells. These results were also confirmed by microscopic examination of the blood smears. The mechanism of the C-Med-100 effect on WBC is not known but other data showing enhanced effects on DNA repair and immune cell proliferative response support a general immune enhancement.

Administration, Oral↗
PubMed1994

[Effect of granulocyte colony stimulating factor (G-CSF) on peripheral blood leukocytes and lymphocytes in patients with chemotherapy-induced leukopenia].

In patients with extensive chemotherapy, G-CSF abrogated leukopenia following administration of cytotoxic agents. Six women with ovarian cancer and chemotherapy-induced leukopenia received 300 micrograms Filgrastrim (r-metHuG-CSF, Neupogen 30; AMGEN, Germany) daily for 10 days. Leukocytes and lymphocyte subsets of peripheral blood were determined before, throughout and after subcutaneous injections of G-CSF by flow cytometry using monoclonal antibodies to CD3, CD4, CD8, CD14, CD16/56, CD19 and CD45. It could be observed that not only neutrophils (23 fold) but also lymphocytes (6 fold) and monocytes (10 fold) showed a dramatic increase in cell counts throughout and after G-CSF administration. This is in contrast to previous reports, where only effects on neutrophils were described. In spite of the increase in lymphocytes the relative percentage of CD3+, CD19+, CD3-CD16/CD56+, CD3+, CD8+ and CD3+ CD4+ lymphocyte subsets did not change throughout and after therapy, except for an increased expression of HLA-DR on CD3+ lymphocytes.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1997

[Immune thrombocytopenia, anemia and leukopenia during pregnancy. Successful therapy with extracorporeal immunoadsorption].

HISTORY AND CLINICAL FINDINGS: A 28-year-old woman in her fourth pregnancy had a positive direct Race-Coombs test in her 14th week of pregnancy. About 6 weeks later she developed marked anaemia, severe thrombocytopenia and leukopenia with nose-bleeds as well as petechiae over the lower abdomen and the inguinal regions. INVESTIGATIONS: Platelet count was 7000/microliter, haemoglobin concentration 4.8 mmol/l (7.73 g/dl) and WBC count 2600/microliter). Bleeding time was markedly prolonged. Erythrocyte-attached immunoglobulin G and complement components as well as antithrombocyte and antigranulocyte antibodies were demonstrated. Haemoblastosis or aplastic anaemia was excluded by bone marrow examination. TREATMENT AND COURSE: The pancytopenia with immune thrombocytopenia, autohaemolytic anaemia and associated leukopenia were classified as Evans syndrome. Administration of glucocorticoids and of immunoglobulins intravenously for 5 days failed to improve the blood picture significantly. But platelet count rose significantly on immunoadsorption (Ig Therasorb columns), allowing the pregnancy to proceed. CONCLUSION: In life-threatening states Ig immunoadsorption can achieve well tolerated, effective and specific elimination of pathogenetically relevant antibodies against blood cells and can also be applied in pregnant women.

Adult↗
PubMed1957

Leukopenia with granulocytopenia in experimental mucormycosis (Rhizopus oryzae infection).

Mucormycosis was produced in rabbits with sustained, severe leukopenia and granulocytopenia induced by repeated injections of nitrogen mustard. Initially, these animals developed extensive fungus lesions at the site of inoculation which later became granulomatous and tended to heal. Only the early phases of host resistance appeared impaired by the virtual elimination of the polymorphonuclear leukocyte as a factor in the host response. Despite the persistent leukopenia and granulocytopenia, the later phases of host resistance resembled those of the normal animal. Thus, the behavior of the infection in this experiment differs greatly from the unchecked progression of mucormycosis in the metabolically abnormal animal with acute alloxan diabetes. The differences in the course of the disease and in the morphologic appearance of the lesions indicate that metabolic alterations in the host affect all phases of host resistance and not only the polymorphonuclear leukocytic response.

Agranulocytosis↗
PubMed1988

Hematologic evaluation of employees with leukopenia. Naval Weapons Center, China Lake, California.

Evaluation of 86 employees with a history of leukopenia at the Naval Weapons Center (NWC), China Lake, California, was done by exposure questionnaires, medical histories, physical examinations, peripheral blood smear, and bone marrow evaluations, including morphologic examination, stem cell culture, and cytogenetics. Forty-eight subjects were found to be leukopenic at the time of the study, and two subjects were found to have hairy cell leukemia. All subjects had positive exposure histories and were healthy at the time of the study. Review of peripheral smears identified the patients with marrow abnormalities. Bone marrow cultures revealed several patients with possible marrow suppression. Chromosome studies were not diagnostic. Five-year follow-up health questionnaires revealed no significant health problems; the two workers with hairy cell leukemia are alive and fully functional. Leukopenia in itself does not appear to be a risk factor for poor health, and it is unknown whether or not it may be a useful screening tool to identify workers at risk in toxic environments. Careful evaluation of blood cell counts and peripheral smears should be sufficient to identify people with potential marrow abnormalities.

Adult↗
PubMed1993

Case report: reversal of severe leukopenia by granulocyte colony-stimulating factor in anorexia nervosa.

Recent attempts to reduce weight by patients with anorexia nervosa have sometimes led to life-threatening hematologic complications. This report describes an instance in which a patient with anorexia nervosa and pancytopenia drastically improved with treatment that included administration of granulocyte colony-stimulating factor. The patient had lost 27 kg of body weight within 8 months. Even after admission, the blood cell count continued to decrease rapidly as follows: platelet, from 244 x 10(3)/microliters to 44 x 10(3)/microliters; erythrocyte, from 4.04 x 10(6)/microliters to 2.58 x 10(6)/microliters; and leukocyte, from 4.8 x 10(3)/microliters to 1.6 x 10(3)/microliters (granulocyte, 0.8 x 10(3)/microliters). Complications included pneumomediastinum, pneumothorax, purpura, petechiae, hepatomegaly, fever, gangrenous stomatitis, and somnolence. Bone marrow aspiration disclosed absence of fat cells, marrow hypoplasia, and infiltration of the mature lymphocytes. Intravenous hyperalimentation, blood transfusion, gamma-globulin, and antibiotics were administered, but leukopenia and fever remained. However, administration of recombinant human granulocyte colony-stimulating factor dramatically reversed the leukopenia and fever. With careful nutrition therapy, the patient's blood cell count and bone marrow normalized by the time of discharge. It was concluded that severe hematologic disorders may occur in patients with anorexia nervosa, and advanced treatment may be required to save the patient's life.

Adolescent↗
PubMed2001

Olanzapine-induced leukopenia with human leukocyte antigen profiling.

Olanzapine is an atypical antipsychotic medication frequently used in the management of psychotic states. While it has proved to be safe compared to clozapine with regard to haematotoxicity, because it has only been available for a few years, full documentation of its haematological side-effects remains incomplete. We report a case of olanzapine-induced leukopenia with associated neutropenia. Since clozapine-induced haematotoxicity has been associated with characteristic human leukocyte antigen (HLA) groups, HLA typing was determined in this patient. Following failure with typical antipsychotic medication, the patient received 10 mg/day of olanzapine. Three weeks later, he developed fever and a significant decrease in leukocyte count. Olanzapine was immediately discontinued. HLA typing was determined. The white cell count returned to normal and the fever, most probably secondary to the low white cell count, subsided with antibiotic treatment. HLA typing results were: A1 24, B7, B35, DRB1*15, DRB1*11, DRB3*01-03, DRB5*01-02. Olanzapine may induce serious leukopenia and neutropenia. HLA typing in this single patient demonstrated a distinct haplotype compared to that previously observed in clozapine-induced haematoxicity.

Clozapine↗
PubMed1978

Acute leukopenia associated with silver sulfadiazine therapy.

A patient with a 30% scald burn was treated with topical silver sulfadiazine (Silvadene). On two occasions, within 48 hours of treatment, the patient developed acute leukopenia. Bone marrow aspiration revealed cell maturation arrest. The possible mechanisms of this leukopenia are discussed. It is recommended that daily leukocyte counts be done in burn patients being treated with silver sulfadiazine.

Acute Disease↗
PubMed1979

Severe leukopenia secondary to carbamazepine administration.

We have reported the first case of severe leukopenia, complicated by infection, associated with the use of carbamazepine. In the literature, most cases of leukopenia secondary to carbamazepine are transient and benign, but any increase in dosage of the drug warrants a close follow-up of blood counts even if previous blood counts were normal.

Adult↗
PubMed1986

Piperacillin-induced anemia and leukopenia.

Piperacillin is being used with increasing frequency as an important antibiotic for the treatment of severe and life-threatening infections. Many of these patients may have multiple possible causes of leukopenia and/or anemia. An awareness of the potential for piperacillin to cause the rapid onset of leukopenia and/or anemia may have important therapeutic implications, especially in severely ill patients.

Adult↗
PubMed1990

Reversible leukopenia related to ciprofloxacin therapy.

In general, ciprofloxacin is well tolerated. The most common adverse effects are nausea, vomiting, diarrhea, dizziness, nervousness, and rash. Reversible leukopenia can be associated with the use of oral ciprofloxacin, as shown by our case. Leukopenia should be watched for as the use of this drug increases.

Ciprofloxacin↗
PubMed2002

KF24345, an adenosine uptake inhibitor, suppresses lipopolysaccharide-induced tumor necrosis factor-alpha production and leukopenia via endogenous adenosine in mice.

3-[1-(6,7-Diethoxy-2-morpholinoquinazolin-4-yl)piperidin-4-yl]-1,6-dimethyl-2,4(1H,3H)-quinazolinedione hydrochloride (KF24345) is a novel potent adenosine uptake inhibitor. KF24345 inhibited [(3)H]adenosine uptake into erythrocytes from human, mouse, rabbit, and hamster with IC(50) values of 59.5, 130.1, 104.2, and 30.9 nM, respectively. In mice, oral administration of KF24345 at 10 mg/kg almost completely inhibited the [(3)H]adenosine uptake into sampled blood cells at least up to 10 h of the administration. In this study, to examine whether the adenosine uptake inhibition exhibits anti-inflammatory effects, we determined the effects of KF24345 on lipopolysaccharide (LPS)-induced tumor necrosis factor-alpha (TNF-alpha) production and leukopenia in mice. KF24345 (10 mg/kg p.o.) significantly suppressed the elevation of serum TNF-alpha concentration after the LPS injection, and the suppressing effect of KF24345 was abolished by the treatment with 4-(2-[7-amino-2-(2-furyl)[1,2,4]triazolo[2,3-a][1,3,5]triazin-5-ylamino]ethyl)phenol, a selective adenosine A(2) receptor antagonist, but not with 8-(noradamantan-3-yl)-1,3-dipropylxanthine, a selective adenosine A(1) receptor antagonist. KF24345 (10 mg/kg p.o.) also inhibited the decrease of leukocytes after the LPS injection, and 8-(p-sulfophenyl)theophylline, a nonselective adenosine receptor antagonist, completely reversed the inhibitory effect of KF24345. These results demonstrate that KF24345 inhibits LPS-induced TNF-alpha production and leukopenia via enhancing the effect of endogenous adenosine. It is thus suggested that the adenosine uptake inhibitor has anti-inflammatory effects in vivo and represents a novel therapeutic approach to the treatment of various inflammatory diseases.

Adenosine↗
PubMed2002

Pathogenesis of pneumococcal pneumonia in cyclophosphamide-induced leukopenia in mice.

Streptococcus pneumoniae pneumonia frequently occurs in leukopenic hosts, and most patients subsequently develop lung injury and septicemia. However, few correlations have been made so far between microbial growth, inflammation, and histopathology of pneumonia in specific leukopenic states. In the present study, the pathogenesis of pneumococcal pneumonia was investigated in mice rendered leukopenic by the immunosuppressor antineoplastic drug cyclophosphamide. Compared to the immunocompetent state, cyclophosphamide-induced leukopenia did not hamper interleukin-1 (IL-1), IL-6, macrophage inflammatory protein-1 (MIP-1), MIP-2, and monocyte chemotactic protein-1 secretion in infected lungs. Leukopenia did not facilitate bacterial dissemination into the bloodstream despite enhanced bacterial proliferation into lung tissues. Pulmonary capillary permeability and edema as well as lung injury were enhanced in leukopenic mice despite the absence of neutrophilic and monocytic infiltration into their lungs, suggesting an important role for bacterial virulence factors and making obvious the fact that neutrophils are ultimately not required for lung injury in this model. Scanning and transmission electron microscopy revealed extensive disruption of alveolar epithelium and a defect in surfactant production, which were associated with alveolar collapse, hemorrhage, and fibrin deposits in alveoli. These results contrast with those observed in immunocompetent animals and indicate that leukopenic hosts suffering from pneumococcal pneumonia are at a higher risk of developing diffuse alveolar damage.

Animals↗